Protective Effects of Microbiome-Derived Inosine on Lipopolysaccharide-Induced Acute Liver Damage and Inflammation in Mice via Mediating the TLR4/NF-κB Pathway,Journal of Agricultural and Food Chemistry

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Protective Effects of Microbiome-Derived Inosine on Lipopolysaccharide-Induced Acute Liver Damage and Inflammation in Mice via Mediating the TLR4/NF-κB Pathway
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2021-06-22 , DOI: 10.1021/acs.jafc.1c01781
Weiling Guo _{1,

2} , Qunran Xiang _{1,

2} , Bingyong Mao _{1,

2} , Xin Tang _{1,

2} , Shumao Cui _{1,

2} , Xiangfei Li ₃ , Jianxin Zhao _{1,

2} , Hao Zhang _{1,

2,

4} , Wei Chen _{1,

2,

4}

Affiliation

This research assessed the anti-inflammatory and hepatoprotective properties of inosine and the associated mechanism. Inosine pretreatment significantly reduced the secretion of several inflammatory factors and serum alanine transaminase (ALT) and aspartate amino transferase (AST) levels in a dose-dependent manner compared with the lipopolysaccharide (LPS) group. In LPS-treated mice, inosine pretreatment significantly reduced the ALT and malondialdehyde (MDA) concentration and significantly elevated the antioxidant enzyme activity. Furthermore, inosine pretreatment significantly altered the relative abundance of the genera, Bifidobacterium, Lachnospiraceae UCG-006, and Muribaculum. Correlation analysis showed that Bifidobacterium and Lachnospiraceae UCG-006 were positively related to the cecal short-chain fatty acids but negatively related to the serum IL-6 and hepatic AST and ALT levels. Notably, inosine pretreatment significantly modulated the hepatic TLR4, MYD88, NF-κB, iNOS, COX2, AMPK, Nfr2, and IκB-α expression. These results suggested that inosine pretreatment alters the intestinal microbiota structure and improves LPS-induced acute liver damage and inflammation through modulating the TLR4/NF-κB signaling pathway.

中文翻译：

微生物组来源的肌苷通过介导 TLR4/NF-κB 通路对脂多糖诱导的小鼠急性肝损伤和炎症的保护作用

该研究评估了肌苷的抗炎和保肝特性及其相关机制。与脂多糖 (LPS) 组相比，肌苷预处理以剂量依赖性方式显着降低了几种炎症因子的分泌和血清丙氨酸转氨酶 (ALT) 和天冬氨酸氨基转移酶 (AST) 水平。在 LPS 处理的小鼠中，肌苷预处理显着降低了 ALT 和丙二醛 (MDA) 浓度，并显着提高了抗氧化酶活性。此外，肌苷预处理显着改变了双歧杆菌属、毛螺菌科UCG-006 和Muribaculum属的相对丰度。相关性分析表明双歧杆菌和毛螺菌科UCG-006 与盲肠短链脂肪酸呈正相关，但与血清 IL-6 和肝脏 AST 和 ALT 水平呈负相关。值得注意的是，肌苷预处理显着调节肝脏 TLR4、MYD88、NF-κB、iNOS、COX2、AMPK、Nfr2 和 IκB-α 的表达。这些结果表明，肌苷预处理通过调节 TLR4/NF-κB 信号通路改变肠道微生物群结构，改善 LPS 诱导的急性肝损伤和炎症。

更新日期：2021-07-14

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